Ppm Carbon Monoxide Research Articles

Comparative Study of Carbon Monoxide Gas Sensing Mechanism for the LTPS MOS Schottky Diodes With Various Metal Oxides

The carbon monoxide (CO) gas sensing mechanism of the Au/MO/n-LTPS MOS Schottky diodes on a glass substrate has been studied with various metal oxides (MO) including SnO2, ZnO, and TiO2 as the sensing element. Because of the deposited SnO2 has the highest band gap and the largest surface to volume ratio morphology, thus leading the Schottky diode with SnO2 to gain the highest relative sensitivity ratio of ~546% to 100 ppm CO ambient under condition of 200°C and -3 V bias. These results are better or comparable to the reported CO sensors. We propose a band gap model to interpret the related sensing mechanism in details.

The low temperature polysilicon (LTPS) thin film MOS Schottky diode on glass substrate for low cost and high performance CO sensing applications

The Au/SnO 2/n-LTPS MOS Schottky diode prepared on a glass substrate for carbon monoxide (CO) sensing applications is studied. The n-LTPS (n-type low temperature polysilicon) is prepared by excimer laser annealing and PH 3 plasma treatment of an amorphous Si thin film on glass substrate. The developed Schottky diode exhibits a high relative response ratio of ∼546% to 100 ppm CO ambient under condition of 200 °C and −3 V bias. The response ratio is better than the reported SnO 2 based resistive type CO sensors of 100% and 37%, respectively on poly-alumina and glass substrates or comparable to 390% of Pt-AlGaN/GaN Schottky diode CO sensor. Thus, the Au/SnO 2/n-LTPS Schottky diode has the potential to develop a low cost high performance CO sensor.

Hydrogen-rich saline reduces delayed neurologic sequelae in experimental carbon monoxide toxicity

We investigated the feasibility and efficacy of hydrogen-rich saline therapy on delayed neurologic sequelae in a rat model of severe acute carbon monoxide (CO) poisoning. Controlled animal study. University research laboratory for Diving Medicine. Sprague-Dawley rats weighing 250 ± 20 g. The rats were exposed to 1000 ppm CO in air for 40 min and then to 3000 ppm for another 20 min until they lost consciousness. Rats were intraperitoneal injected with hydrogen-rich saline or normal saline (10 mL/kg) for six times after resuscitation at 0, 12, 24, 36, 48, and 60 hrs, respectively. The rats without CO poisoning were used as normal controls. Brain tissue inflammation, cell death, and cognitive dysfunction were observed at one week after CO poisoning. Hydrogen-rich saline treatment significantly reduced the level of degraded myelin basic protein, decreased the expression of ionized calcium-binding adapter molecule 1, Iba1, a microglial marker, reduced DNA oxidation, and suppressed proinflammatory cytokine interleukin-1β, interleukin-6, and tumor necrosis factor-α in the cortex and hippocampal tissues when compared with those in normal saline-treated rats. These histologic and biological improvements were accompanied with an improvement in the Morris water maze test. This observation demonstrated that hydrogen-rich saline peritoneal injection improves histologic and functional assessment in a rat model of CO encephalopathy. Hydrogen saline has potentials as a novel and alternative therapy for severely CO-poisoned patients with delayed neurologic sequelae. The therapeutic effects of hydrogen-rich saline may be related to antioxidant and anti-inflammatory actions.

Synthesis and CO Gas-Sensing Properties of CuO and Spinel Ferrite Nanocomposite Thin Films

A nanocomposite thin film composed of tenorite (CuO) and spinel ferrite (CuxFe3−xO45 has been prepared by radio-frequency sputtering method followed by a post-deposition thermal annealing. The nanostructure was examined by grazing X-ray diffraction, atomic force microscopy and scanning electron microscopy. CuO-CuxFe3−xO4 nanocomposite layer was deposited on the top of screenprinted gold electrodes onto SiO2(200 nm)/Si substrate. It was found that this material contains p–n nano-heterojunctions, was sensitive to 500 ppm carbon monoxide at the operational temperature of 400 °C and exhibited a large response of 90%.

Investigations of a platinum–ruthenium/carbon nanotube catalyst formed by a two-step spontaneous deposition method

Platinum (Pt) is a popular catalyst for hydrogen oxidation on the anode side of solid polymer fuel cells (SPFC). It increases the electrode activity, which catalyzes the reaction of the fuel cell. There are two methods commonly used to produce hydrogen for SPFC: fuel reforming and methanol decomposition. Both of these methods produce carbon monoxide, which is considered to be a poison for SPFC because it deactivates Pt easily. Adding ruthenium (Ru) to a Pt catalyst is an efficient way to improve the inhibition of carbon monoxide (CO) formation and reduce the Pt loading requirement. This study introduces a method to synthesize a bimetal catalyst that is suitable for SPFC. To improve the electrocatalyst activity, a new process with two spontaneous deposition steps is adopted. In the first step, Ru is deposited on the wall of carbon nanotubes (CNTs) to obtain Ru/CNTs. Pt is then added in the second deposition step to form Pt–Ru/CNTs. The morphology and microstructure of catalysts are characterized with microscopes, and the performance of membrane electrode assembly is evaluated by cyclic voltammetry method. Experimental results have proved that even with a lower Pt loading, this home-brewed bimetal catalyst performs a compatible electrocatalytic activity, and is capable of resisting attack from CO when a syngas (H 2 + 20 ppm CO) is provided.

Existence of a threshold for hydroxyl radical generation independent of hypoxia in rat striatum during carbon monoxide poisoning

We examined the role of hypoxia in the carbon monoxide (CO)-induced generation of the hydroxyl radical (•OH) in the striatum, which could contribute to brain damage due to CO poisoning. Exposure of free-moving rats to 1,000 and 3,000 ppm CO or 8 and 5% O2 for 40 min caused concentration-dependent hypoxic conditions in terms of carboxyhemoglobin (COHb), deoxyhemoglobin, oxyhemoglobin, and O2 contents in arterial blood. The hypoxic conditions seemed comparable between 3,000 ppm CO and 5% O2, although alterations of pH and partial O2 pressure (PO2) were complex and concentration independent. In the striatum, CO and low O2 decreased tissue PO2 levels in a concentration-dependent and concentration-independent manner, respectively, but levels at the end of exposure were comparable among all groups. This was also the case for the increase in striatal blood flow. Although the increases in extracellular glutamate (excitatory), taurine (inhibitory), and alanine (non-neurotransmitter), in the striatum in response to CO and low O2 were complex, 3,000 ppm CO and 5% O2 had comparable effects. Thus, 3,000 ppm CO and 5% O2 seemed to induce comparable hypoxic conditions. Nevertheless, the former more strongly stimulated (•OH generation in the striatum than the latter. In addition, in contrast to low O2 which caused a concentration-dependent increase in (•OH, 1,000 ppm CO had no effect. The findings suggest that striatal •OH generation due to CO poisoning may be independent of hypoxia per se and that a threshold might exist.

Protection against lung graft injury from brain-dead donors with carbon monoxide, biliverdin, or both

The process of brain death can induce acute lung injury in donors and aggravate ischemia-reperfusion injury in grafts. Carbon monoxide (CO) and biliverdin (BV) have been shown to attenuate ischemia-reperfusion injury. We therefore examined if the administration of both CO and BV provide enhanced cytoprotection against lung graft injury from brain-dead (BD) rat donors. Brain death was induced in all donors, after which they were observed for 1.5 hours and then underwent lung transplantation. The recipients were ventilated with 40% oxygen (control group), ventilated with 250 ppm CO in 40% oxygen (CO group), treated with BV (35 mg/kg) intraperitoneally (BV group), or treated with CO and BV conjointly (COBV group) before transplantation (n = 8 each group). The recipients were sacrificed 2 hours after lung transplantation by exsanguination. Serum levels of interleukin (IL)-8 and tumor necrosis factor (TNF)-α were measured by enzyme-linked immunosorbent assay. CO and/or BV treatment attenuated partial pressure of arterial oxygen (Pao(2))/fraction of inspired oxygen (Fio(2)) aggravation in the recipients after reperfusion, reduced the wet weight/dry weight ratio, decreased the lung injury score, inhibited the activity of myeloperoxidase in grafts, and decreased serum levels of IL-8 and TNF-α compared with the control group (p < 0.05). The COBV group had significantly decreased malonaldehyde levels and increased superoxide dismutase levels in lung grafts compared with the CO group (p < 0.05). The static pressure-volume curve of the lungs was ameliorated in the CO group, BV group, and COBV group compared with the control group (p < 0.05). CO and BV exert protective effects through anti-inflammatory and anti-oxidant mechanisms, and dual treatment provided enhanced cytoprotection against lung graft injury from BD rat donors.

Carbon Monoxide Therapy Reduces Reactive Oxygen Species Production and the Short-Term Hematopoietic Stem Cell Population In Heme-Oxygenase-1 Knockout Mice

AbstractAbstract 4767Previous studies have demonstrated that heme-oxygenase-1 (HO-1), the rate limiting enzyme in the catabolism of heme, is a regulator of the balance between hematopoiesis and stem cell preservation under stress. HO-1 produces three by-products, carbon monoxide, biliverdin/bilirubin, and iron/ferritin, all of which have demonstrated antioxidant and anti-apoptotic properties. HO-1-/- mice display oxidative stress, anemia, and leukocytosis with chronic inflammation. We hypothesize that therapy with inhaled carbon monoxide (CO) may reduce stress hematopoiesis in HO-1-/- mice, restoring them to normal hematopoiesis. We have previously reported that treatment with 250 ppm CO for 1 h raises mouse carboxyhemoglobin to 14–20% which returns to baseline within 24 hours. Therefore, in order to test this hypothesis we treated 25 week old HO-1-/- mice and HO-1+/+ mice (n=7/strain) with 250 ppm inhaled CO for 1 h/day, 3 days/week for eight weeks and compared them to an equal number of untreated HO-1-/- and HO-1+/+ mice. We demonstrate that after four weeks, CO-treated HO-1-/- mice have a total white blood cell count of 11.9 ± 3.2 K/μ L compared to 22.6 ± 3.2 K/μ L in untreated HO-1-/- mice (p<0.05), with HO-1+/+ mice having no treatment effect. After 8-weeks of treatment the mice were sacrificed and methylcellulose colony-forming unit assays and flow cytometry were performed on bone marrow to assess their hematopoietic potential. Total methylcellulose colony-forming units were similar in both HO-1-/- and HO-1+/+ mice with CO-treatments significantly (p<0.05) increasing the total number of colonies per animal. Of note, in both the CO-treated HO-1-/- and HO-1+/+ mice the CFU-GM were not significantly affected. Cell cycle analysis of the bone marrow using propidium iodide demonstrates that untreated HO-1-/- mice have a significantly decreased percent of cells in S-phase compared to untreated HO-1+/+ mice. Treatment with CO significantly (p<0.05) increases the percent of cells in S-phase in HO-1-/- mice but not HO-1+/+ mice. Similarly, untreated HO-1-/- mice have a lower frequency of cells in sub-G1 phase compared to untreated HO-1+/+ mice, however CO-treatments significantly (p<0.01) increase this frequency in HO-1-/- mice to levels comparable with untreated and CO-treated HO-1+/+ mice. Reactive oxygen species (ROS) production in lineage-, c-kit+, Sca-1+ (KLS) cell population was assessed using 5-(and 6-)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate dye. HO-1-/- mice have a significantly (p<0.001) increased proportion of ROS positive KLS cells compared with HO-1+/+ mice. Interestingly, the CO-treated HO-1-/- mice had a significantly higher proportion of KLS cells staining positive for ROS, but the mean fluorescent intensity of this population was significantly (p<0.05) decreased compared to untreated HO-1-/- mice. This indicates that there is an overall decrease in ROS in the KLS cells of CO-treated HO-1-/- mice compared to untreated HO-1-/- mice. Analysis of long-term, short-term, and multipotent progenitor cell populations was conducted and reveals significant changes at the level of the short-term hematopoietic progenitor population (ST-HSC). Specifically, untreated HO-1-/- mice have a significantly increased percent of ST-HSC cells compared to untreated HO-1+/+ mice. Treatment with CO significantly (p<0.05) decreases the percent of ST-HSC cells in HO-1-/- mice but not HO-1+/+ mice. Combined this data indicates that CO therapy is able to modify the hematopoietic potential of HO-1-/- mice. We propose a model in which CO-mediated signaling initiates a homeostatic conditioning program in stem cells to balance hematopoiesis and stem cell preservation. Disclosures:Belcher:Sangart: Research Funding. Vercellotti:Sangart: Consultancy, Research Funding.

The Impact of sub ppm Carbon Monoxide and ppm Level CO/Toluene and Methylcyclohexane/CO Mixtures on PEMFC Performance and Durability

This work studied the effects that exposure to the hydrogen fuel impurities: carbon monoxide (CO), toluene and methylcyclohexane (MeCH) had on the performance and durability of GORE{trade mark, serif} PRIMEA® MESGA (A510.1/M710.18/C510.4) membrane electrode assemblies (MEAs) used in hydrogen proton exchange membrane fuel cells (PEMFCs). MEAs used in this work had anode platinum catalyst loadings of 0.1 mg Pt cm-2 and were subjected to both single impurities and impurity mixtures. Gas chromatography was used to study the magnitude of conversion for CO to carbon dioxide (CO2) and toluene to MeCH.

Carbon monoxide inhalation decreased lung injury via anti-inflammatory and anti-apoptotic effects in brain death rats

Brain death (BD) induces acute lung injury and makes donor lungs unfit for transplantation. Carbon monoxide (CO) inhalation at 50-500 ppm exerts anti-inflammatory and anti-apoptosis effects in several lung injury models. We examined whether CO inhalation would show favorable effects on lung injury in BD rats. BD rats inhaled 250 ppm CO for two hours. Inhalation decreased the severity of lung injury, as checked by histological examination. CO treatment reversed aggravation in PaO(2)/FiO(2), base excess and pH of BD rats. CO inhalation downregulated the pro-inflammatory cytokines (tumor necrosis factor-α, interleukin-6), and inhibited activity of myeloperoxidase in lung tissue. Inhalation significantly decreased cell apoptosis of lungs, and inhibited mRNA expression of intercellular adhesion molecule-1 and caspase-3 in the lungs. Further, the inhalation activated phosphorylation of p38 expression and inhibited phosphorylation of extracellular signal-regulated kinase expression in the lungs. In conclusion, CO exerts potent protective effects on lungs from BD rats, exhibiting anti-inflammatory and anti-apoptosis functions by modulating the mitogen-activated protein kinase signal transduction.

The time-dependent protective effect of hyperbaric oxygen on neuronal cell apoptosis in carbon monoxide poisoning

Introduction: The progressive clinical course with delayed neurological damage in carbon monoxide (CO) poisoning may be due to neuron apoptosis. The usefulness of hyperbaric oxygen (HBO) in different time periods after CO exposure in neuronal cell apoptosis reduction has not been evaluated thus far. The aim was to evaluate HBO efficacy in reducing neuronal apoptosis in different time periods after CO exposure.Methods: Wistar rats were exposed to 3000 ppm CO in air for 60 min and 100% oxygen at a pressure of three bar for 30 min 0–12 h after CO exposure. The apoptosis was evaluated by immunohistochemical analysis with antibodies against activated caspase-3 and the percentage of caspase-3 positive hippocampal ganglionic cells was reported.Results: It was shown that CO poisoning results in ganglionic cell apoptosis. The percentage of apoptotic cells in rats exposed to CO was the highest (32%), whereas the percentage of apoptotic cells in rats exposed to HBO 0 and 1 h after CO was similar with a lower percentage than rats exposed to CO. The percentage of apoptotic cells in rats exposed to HBO 3 and 5 h after CO was similar with a lower percentage than rats exposed to HBO 0 and 1 h after CO. The percentage of apoptotic cells in rats exposed to HBO 7–12 h after CO was similar with a higher percentage than rats exposed to HBO 5 h after CO.Conclusion: HBO has a time-dependent protective effect on CO-induced neuron apoptosis with the highest efficiency at 3 and 5 h after CO poisoning.

Ambient air pollution exposure and full-term birth weight in California

BackgroundStudies have identified relationships between air pollution and birth weight, but have been inconsistent in identifying individual pollutants inversely associated with birth weight or elucidating susceptibility of the fetus by trimester of exposure. We examined effects of prenatal ambient pollution exposure on average birth weight and risk of low birth weight in full-term births.MethodsWe estimated average ambient air pollutant concentrations throughout pregnancy in the neighborhoods of women who delivered term singleton live births between 1996 and 2006 in California. We adjusted effect estimates of air pollutants on birth weight for infant characteristics, maternal characteristics, neighborhood socioeconomic factors, and year and season of birth.Results3,545,177 singleton births had monitoring for at least one air pollutant within a 10 km radius of the tract or ZIP Code of the mother's residence. In multivariate models, pollutants were associated with decreased birth weight; -5.4 grams (95% confidence interval -6.8 g, -4.1 g) per ppm carbon monoxide, -9.0 g (-9.6 g, -8.4 g) per pphm nitrogen dioxide, -5.7 g (-6.6 g, -4.9 g) per pphm ozone, -7.7 g (-7.9 g, -6.6 g) per 10 μg/m3 particulate matter under 10 μm, -12.8 g (-14.3 g, -11.3 g) per 10 μg/m3 particulate matter under 2.5 μm, and -9.3 g (-10.7 g, -7.9 g) per 10 μg/m3 of coarse particulate matter. With the exception of carbon monoxide, estimates were largely unchanged after controlling for co-pollutants. Effect estimates for the third trimester largely reflect the results seen from full pregnancy exposure estimates; greater variation in results is seen in effect estimates specific to the first and second trimesters.ConclusionsThis study indicates that maternal exposure to ambient air pollution results in modestly lower infant birth weight. A small decline in birth weight is unlikely to have clinical relevance for individual infants, and there is debate about whether a small shift in the population distribution of birth weight has broader health implications. However, the ubiquity of air pollution exposures, the responsiveness of pollutant levels to regulation, and the fact that the highest pollution levels in California are lower than those regularly experienced in other countries suggest that precautionary efforts to reduce pollutants may be beneficial for infant health from a population perspective.

The Effects of the Location of Au Additives on Combustion-generated SnO2 Nanopowders for CO Gas Sensing

The current work presents the results of an experimental study of the effects of the location of gold additives on the performance of combustion-generated tin dioxide (SnO2) nanopowders in solid state gas sensors. The time response and sensor response to 500 ppm carbon monoxide is reported for a range of gold additive/SnO2 film architectures including the use of colloidal, sputtered, and combustion-generated Au additives. The opportunities afforded by combustion synthesis to affect the SnO2/additive morphology are demonstrated. The best sensor performance in terms of sensor response (S) and time response (τ) was observed when the Au additives were restricted to the outermost layer of the gas-sensing film. Further improvement was observed in the sensor response and time response when the Au additives were dispersed throughout the outermost layer of the film, where S = 11.3 and τ = 51 s, as opposed to Au localized at the surface, where S = 6.1 and τ = 60 s.

Efficacy and Safety of Inhaled Carbon Monoxide during Pulmonary Inflammation in Mice

BackgroundPulmonary inflammation is a major contributor to morbidity in a variety of respiratory disorders, but treatment options are limited. Here we investigate the efficacy, safety and mechanism of action of low dose inhaled carbon monoxide (CO) using a mouse model of lipopolysaccharide (LPS)-induced pulmonary inflammation.MethodologyMice were exposed to 0–500 ppm inhaled CO for periods of up to 24 hours prior to and following intratracheal instillation of 10 ng LPS. Animals were sacrificed and assessed for intraalveolar neutrophil influx and cytokine levels, flow cytometric determination of neutrophil number and activation in blood, lung and lavage fluid samples, or neutrophil mobilisation from bone marrow.Principal FindingsWhen administered for 24 hours both before and after LPS, inhaled CO of 100 ppm or more reduced intraalveolar neutrophil infiltration by 40–50%, although doses above 100 ppm were associated with either high carboxyhemoglobin, weight loss or reduced physical activity. This anti-inflammatory effect of CO did not require pre-exposure before induction of injury. 100 ppm CO exposure attenuated neutrophil sequestration within the pulmonary vasculature as well as LPS-induced neutrophilia at 6 hours after LPS, likely due to abrogation of neutrophil mobilisation from bone marrow. In contrast to such apparently beneficial effects, 100 ppm inhaled CO induced an increase in pulmonary barrier permeability as determined by lavage fluid protein content and translocation of labelled albumin from blood to the alveolar space.ConclusionsOverall, these data confirm some protective role for inhaled CO during pulmonary inflammation, although this required a dose that produced carboxyhemoglobin values close to potentially toxic levels for humans, and increased lung permeability.

An Inhalation Chamber Model for Controlled Studies of Tobacco Smoke Toxicity in Rodents

Introduction Smoking is a serious worldwide public health problem. Animal models act as a bridge between laboratory and human studies. The models applied are difficult to reproduce because of the use of different types of inhalation chambers and mainly because of the lack of continuous monitoring of smoke concentration. Objective To develop an inhalation chamber for rats (with only the nose exposed) in which the amount of carbon monoxide (CO) can be maintained and monitored constantly. Material and methods Male Wistar rats weighing 250 g were exposed to 50 ppm CO produced by the smoke from a filter-free cigarette. The animals were submitted to a single 2-h exposure and then sacrificed at 0, 4, 24 and 48 h. The control group was left restrained inside the small perpendicular chambers, receiving only 5 L/min of compressed air. Results The model was able to increase HbCO levels immediately after the end of exposure ( p < 0.001), with a decrease being observed from 2 h onwards when compared to the levels of the control group. Plasma cotinine increased immediately after exposure, and showed still detectable levels at 2 and 4 h ( p < 0.05). Conclusion We conclude that the presented inhalation chamber system is able to maintain a controlled CO concentration in a model in which small animals are exposed to the inhalation of cigarette smoke, permitting well-controlled studies, as well as investigations involving other toxic gases and air pollutants.

The role of heart-type fatty acid-binding protein in the evaluation of carbon monoxide poisoning in rats

Acute carbon monoxide (CO) poisoning can cause early and persistent damages in tissues sensitive to hypoxia. This study investigated serum heart-type fatty acid-binding protein (H-FABP) levels as a biomarker of acute CO poisoning in rats. The rats were exposed to a mixture of either 3000 (group A) or 5000 (group B) parts per million (ppm) CO in air, or to ambient air (group C, control group). Blood samples were taken just before, immediately after and 6 hours after the exposure, and serum H-FABP and troponin-I levels were measured. The consciousness level was evaluated just after the exposure. The survival rate was monitored for 7 days. Serum H-FABP levels increased just after the CO exposure in both groups A and B. Additionally, H-FABP level was higher in group B than in group A, immediately after the exposure. However, serum troponin-I levels only increased at 6 hours after the CO exposure in groups A and B. Consciousness and survival rates in group B were lower than that in group A. Our results suggest that H-FABP might have potential to be an early and quantitative parameter of clinical severity and prognosis in CO poisoning.

A single dose of carbon monoxide intraperitoneal administration protects rat intestine from injury induced by lipopolysaccharide.

Treatment with inhaled carbon monoxide (CO) has been shown to ameliorate intestinal injury induced by lipopolysaccharide (LPS) or ischemia-reperfusion in experimental animals. We hypothesized that CO intraperitoneal administration (i.p) might provide similar protection against inhaled gas. In the present study, 1 h after intravenously receiving 5 mg/kg LPS, rats were exposed to either room air or 2 ml/kg of 250 ppm CO i.p for 1, 3, and 6 h. Intestinal tissues were collected to determine the levels of platelet activator factor (PAF), intercellular adhesion molecule-1 (ICAM-1), interleukin-10 (IL-10), maleic dialdehyde (MDA), cell apoptotic rate and the phosphorylated p38 mitogen activated protein kinase (MAPK), as well as myeloperoxidase (MPO) and superoxide dismutase (SOD) activity. After CO i.p, the increase of PAF, ICAM-1, MDA, MPO, and cell apoptosis rate induced by LPS was markedly reduced (P < 0.05 or 0.01), while the decrease of IL-10 and SOD was significantly increased (P < 0.05). Western blotting showed that the effects of CO i.p were mediated by p38 MAPK pathway. Thus, the results of our study show that CO i.p exerts potent protection against LPS induced injury to the intestine via anti-oxidant, anti-inflammation and anti-apoptosis, which may involve the p38 MAPK pathway.

Cobalt Oxide Nanosheet and CNT Micro Carbon Monoxide Sensor Integrated with Readout Circuit on Chip

The study presents a micro carbon monoxide (CO) sensor integrated with a readout circuit-on-a-chip manufactured by the commercial 0.35 μm complementary metal oxide semiconductor (CMOS) process and a post-process. The sensing film of the sensor is a composite cobalt oxide nanosheet and carbon nanotube (CoOOH/CNT) film that is prepared by a precipitation-oxidation method. The structure of the CO sensor is composed of a polysilicon resistor and a sensing film. The sensor, which is of a resistive type, changes its resistance when the sensing film adsorbs or desorbs CO gas. The readout circuit is used to convert the sensor resistance into the voltage output. The post-processing of the sensor includes etching the sacrificial layers and coating the sensing film. The advantages of the sensor include room temperature operation, short response/recovery times and easy post-processing. Experimental results show that the sensitivity of the CO sensor is about 0.19 mV/ppm, and the response and recovery times are 23 s and 34 s for 200 ppm CO, respectively.

Helium Chemistry for Very High Temperature Reactors

Chemical impurity contained in the coolant helium of Very High Temperature Reactors (VHTRs) affects not only the deterioration of mechanical strength caused by decarburization of the high-temperature materials utilized at the heat transfer tubes of the Intermediate Heat Exchanger (IHX) but also the deterioration of heat transfer efficiency caused by carbon deposition, which could occur at the surface of the heat transfer tubes. Such deterioration results in the shortening of the lifetime of high-temperature equipment. Since the helium purification technology applied in past high-temperature gas-cooled reactors can only maintain the core integrity by limiting the oxidation of graphite, it is necessary to establish a control technology in order to maintain the mechanical strength as well as heat transfer efficiency of hightemperature equipment. In this study, carbon deposition that could occur at the surface of the heat transfer tubes of theIHX and decarburization of Hastelloy XR used at the heat transfer tubes were evaluated by referring to the actual chemistry data obtained by the HTTR. Also, the chemical composition to be maintained during a reactor operation was proposed by evaluating not only the core graphite oxidation but also carbon deposition and decarburization. It was identified that when the chemical composition could not be maintained adequately, the injection of 10 ppm carbon monoxide could effectively control the chemical composition towards the designated area at the chromium stability diagram where the stable oxidized layer would be generated sufficiently. The proposed chemistry control technology is expected to contribute to the economy of the purification systems of future VHTRs.

The Impact of sub ppm Carbon Monoxide and ppm Level CO/Toluene and Methylcyclohexane/CO Mixtures on PEMFC Performance and Durability

not Available.